Neuropsychiatric disorders in preeclampsia (PE) women are prevalent and worsen PE outcome. Immune-related biomarkers including soluble sCD80 and cytotoxic T-lymphocyte antigen-4 (sCTLA-4) are not well studied in relation to depression, anxiety, and chronic fatigue due to PE.

The aim is to study serum immune-inflammatory biomarkers of PE and delineate their associations with the Hamilton Depression (HAMD), Anxiety (HAMA), and Fibro-Fatigue (FF) rating Scale scores. sCD80, sCTLA-4, vitamin D, granulocyte-macrophage colony-stimulating factor, zinc, copper, magnesium, and calcium were measured in 90 PE compared with 60 non-PE pregnant women.

PE women show higher depression, anxiety and FF rating scale scores as compared with control women. sCTLA-4, sCD80, and copper were significantly higher and zinc, magnesium, and calcium significantly lower in PE women than in controls. Multiple regression analysis showed that around 55.8%-58.0% of the variance in the HAMD, HAMA and FF scores was explained by the regression on biomarkers; the top 3 most important biomarkers were sCTLA-4, sCD80, and vitamin D. The sCTLA-4/sCD80 ratio was significantly and inversely associated with the HAMD/HAMA/FF scores. We found that around 70% of the variance in systolic blood pressure could be explained by sCTLA-4, vitamin D, calcium, and copper.

The findings underscore that PE and depression, anxiety, and chronic fatigue symptoms due to PE are accompanied by activation of the immune-inflammatory response system. More specifically, disbalances among soluble checkpoint molecules seem to be involved in the pathophysiology of hypertension and neuropsychiatric symptoms due to PE.

Non-adherence and negative attitudes towards medication are major problems in treating psychotic disorders. Cytochrome P450 2D6 (CYP2D6) contributes to the metabolism of aripiprazole and risperidone. Variations in CYP2D6 activity may affect treatment response or adverse effects. The impact of these variations on adherence and medication attitudes is unclear.

This study investigates the relationships between CYP2D6 phenotype, self-reported adherence, adverse effects, and attitudes among aripiprazole and risperidone users.

This study analyzed data from the SUPER-Finland cohort of 10,474 adults with psychotic episodes, including 1,429 aripiprazole and 828 risperidone users. The Attitudes towards neuroleptic treatment (ANT) questionnaire assessed adherence and adverse effects in all patients, while medication-related attitudes were examined in a subgroup of 1,000 participants. Associations between CYP2D6 phenotypes and outcomes were analyzed using logistic regression and beta regression in aripiprazole and risperidone groups separately.

Among risperidone users, we observed no association between CYP2D6 phenotypes and adherence, adverse effects, or attitudes. Similarly, no link was found between adherence and CYP2D6 phenotypes among aripiprazole users. However, aripiprazole users with the ultrarapid CYP2D6 phenotype had more adverse effects (OR = 1.71, 95 % CI 1.03–2.90, p = 0.041). Among aripiprazole users, CYP2D6 ultrarapid phenotype was associated with less favorable attitudes towards antipsychotic treatment (β = -0.48, p = 0.023).

We found preliminary evidence that the ultrarapid CYP2D6 phenotype is associated with increased adverse effects and negative attitudes towards antipsychotic medication among aripiprazole users. CYP2D6 phenotype did not influence adherence, adverse effects, or attitudes among risperidone users.

New developments in neuro-navigation and machine learning have allowed for personalized approaches to repetitive transcranial magnetic stimulation (rTMS) to treat various neuropsychiatric disorders. One specific approach, known as the Cingulum Framework, identifies individualized brain parcellations from resting state fMRI based on a machine-learning algorithm. Theta burst stimulation, a more rapid form of rTMS, is then delivered for 25 sessions, 5 per day, over 5 days consecutively or spaced out over 10 days. Preliminary studies have documented this approach for various neurological and psychiatric ailments. However, the safety and tolerability of this approach is unclear.

We performed a retrospective study on 165 unique patients (202 Target Sets) treated with this personalized approach between January 2020 to December 2023.

Common side effects included fatigue (102/202, 50%), local muscle twitching (89/202, 43%), headaches (49/202, 23%), and discomfort (31/202, 17%), all transient. The top 10 unique parcellations commonly found in the Target Sets included L8av (52%), LPGs (28%), LTe1m (21%), RTe1m (18%), LPFM (17%), Ls6-8 (13%), Rs6-8 (9%), L46 (7%), L1 (6%), and L6v (6%). Fatigue was most common in Target Sets that contained R6v (6/6, 100%) and L8c (5/5, 100%). Muscle twitches were most common in Target Sets that contained RTGv (5/5, 100%) and LTGv (4/4, 100%).

These side effects were all transient and well-tolerated. No serious side effects were recorded. Results suggested that individualized, connectome-guided rTMS is safe and contain side effect profiles similar to other TMS approaches reported in the literature.

Selective serotonin reuptake inhibitors (SSRIs) have been associated with increased risk of osteoporosis, and sertraline may be more potent than citalopram in this regard. Here, target trial emulation was used to investigate whether sertraline, citalopram and escitalopram (the S-enantiomer of citalopram) differentially affect the risk of osteoporosis. Subsequently, it was examined whether SSRIs increase the risk of osteoporosis in a dose-response-like manner.

Danish nationwide registers were used to identify all individuals that initiated treatment for depression with sertraline, citalopram, or escitalopram between January 1, 2007, and March 1, 2019. These individuals were followed until development of osteoporosis, death, or end of follow-up. Cox proportional hazards regression was used to adjust for relevant baseline covariates to emulate randomised treatment allocation to compare the rate of osteoporosis for individuals treated with sertraline, citalopram or escitalopram. Subsequently, the cumulative dose of sertraline, citalopram, and escitalopram was calculated, and Cox proportional hazards regression was used to assess dose-response-like relationships with osteoporosis.

We identified 27,280, 65,529, and 17,703 individuals initiating treatment with sertraline, citalopram, and escitalopram, respectively. There was no material or statistically significant differential risk of osteoporosis between these groups (adjusted hazard rate ratio, aHRR = 0.98 for citalopram versus sertraline and aHRR = 0.94 for escitalopram versus sertraline). The results were not indicative of the SSRIs having a dose-response-like effect on osteoporosis risk.

Sertraline, citalopram and escitalopram do not appear to differentially affect the risk of osteoporosis. The lack of clear dose-response-like relationships suggest that they do not have a causal effect on osteoporosis risk.

Extant literature implicates the role of glucagon-like peptide-1 (GLP-1) and GLP-1 receptor agonists (GLP-1RAs) on modulating alcohol-associated behaviours, with a particular emphasis of these agents on neural circuits subserving reward and appetite control. Herein, we explore the potential effects of GLP-1RAs on alcohol-associated behaviours in brain regions implicated in reward processing facilitating the repurposing of these agents for the treatment and prevention of problematic drinking. Understanding how GLP-1’s analogues interact with alcohol-related behaviours may underscore the development of therapeutic strategies for alcohol use disorder (AUD) and those with comorbid metabolic disorders.

A systematic review was conducted, wherein relevant literature was identified through Web of Science, PubMed, and OVID (MedLINE, Embase, AMED, PsycInfo, JBI EBP) from database inception to October 27th, 2024. Preclinical and clinical studies examining the association between GLP-1RAs and alcohol-related behaviours were assessed.

Preclinical studies (n = 19) indicate that GLP-1RAs attenuate alcohol-related behaviours, with exenatide demonstrating significant dose-dependent effects in high alcohol-consuming phenotypes. Semaglutide and liraglutide are associated with reduced alcohol intake, though their effects were often transient. In human studies (n = 2) with AUD, semaglutide significantly reduced alcohol consumption, while exenatide showed mixed results, with reductions in alcohol drinking within high BMI subpopulations.

Extant preclinical and clinical literature provides preliminary support for the potential therapeutic role of GLP-1RAs in attenuating alcohol consumption and preference. There is a need for large well controlled studies evaluating the effect of GLP-1RAs as a treatment strategy for behavioural modifications in individuals living with alcohol use disorder.

Glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-1 receptor agonist (GLP-1 RA) administration has been associated with neuroproliferative effects and modulatory effects in neuronal pathways. Herein, we conducted a comprehensive synthesis of the effects of GLP-1 and GLP-1 RAs on neurogenesis.

We examined studies that investigate changes in neurogenesis mediated by GLP-1 and GLP-1 RA administration in both human and animal populations. Relevant articles were retrieved through OVID (MedLine, Embase, AMED, PsychINFO, JBI EBP Database), PubMed, and Web of Science from database inception to July 2nd. Primary studies investigating the role of GLP-1 and GLP-1 RAs on neurogenesis were included for analysis.

GLP-1 and GLP-1 RAs (i.e. exenatide, geniposide, liraglutide, lixisenatide, and semaglutide), increased neurogenesis within the dentate gyrus, hippocampus, olfactory bulb, and the medial striatum in animal models. Additionally, GLP-1 and GLP-1 RAs were associated with modulating changes in multiple apoptotic pathways and upregulating survival pathways.

GLP-1 and GLP-1 RAs are positively associated with neurogenesis. This effect may have translational implications insofar as disparate mental disorders that are characterised by neurogenesis defects (e.g. depressive disorders and neurocognitive disorders) may be benefitted by these agents.

This study aimed to utilise graph theory to explore the functional brain networks in individuals with tic disorders and to investigate resting-state functional connectivity changes in critical brain regions associated with tic disorders.

Participants comprised individuals with tic disorders and age-matched healthy controls, ranging from 6 to 18 years old, all recruited from Korea University Guro Hospital. We ensured a medication-naïve cohort by excluding participants exposed to psychotropic medications for at least three weeks prior to the study. Data included structural and resting-state functional MRI scans, analysed with the CONN-fMRI Functional Connectivity toolbox v20b. The analysis included 22 patients (18 males, 4 females) and 26 controls (14 males, 12 females).

Significantly increased global efficiency was observed in the left inferior frontal gyrus pars opercularis among tic disorder patients compared to controls. Furthermore, this region displayed enhanced resting-state functional connectivity with its right counterpart in patients versus controls.

The inferior frontal gyrus pars opercularis, known for its inhibitory role, may reflect adaptive functional adjustments in response to tic symptoms. Increased hubness of the inferior frontal gyrus pars opercularis possibly represents functional adjustments in response to tic symptoms. The identified brain region with increased efficiency and connectivity presents a promising avenue for further research into tic expression and control mechanisms.

Ultrasonic vocalisations (USVs) emitted by rats may reflect affective states. Specifically, 50 kHz calls emitted during juvenile playing are associated with positive affect. Given that depression is characterised by profound alterations in this domain, we proposed that USV calls may configure a suitable tool for assessing depressive-like states. Utilising the Flinders Sensitive Line (FSL), a well-established animal model of depression, we assessed USV calls emitted by rats during tickling, a procedure based on juvenile rats’ rough-and-tumble play.

Juvenile FSL rats and their control counterparts, the Flinders Resistant Line (FRL) and Sprague Dawley, were submitted to tickling sessions to imitate rats playing behaviour. The rats were tickled daily for 6 weeks starting at PND21. Tickling sessions were recorded for further acoustic analysis of 50 kHz calls.

Tickling increased 50 kHz calls in all the strains. FSL rats emitted more calls than control strains and exhibited a higher number of flat-trill combination calls.

Tickling is a robust method for inducing 50 kHz USV calls. Analysing USV calls emitted during tickling configurates a suitable method for studying affective states relevant to depression. FSL rats did not present anhedonia but rather higher reward sensitivity, which may underlie their stress vulnerability.

Folate and cobalamin deficiency or impaired function due to genetic variants in key enzymes have been associated with neuropsychiatric symptoms. The aim of this study was to compare folate and cobalamin status in patients admitted to an acute psychiatric unit to patients from primary health care in order to reveal factors which may be important in the follow-up of patients with mental disorders.

Anonymous blood samples tested for folate, cobalamin, the metabolic marker total homocysteine (tHcy), creatinine and glomerular filtration rate as well as age and gender in patients admitted to a psychiatric acute unit (n = 981) and patients from primary health care (controls) (n = 32,201) were reviewed retrospectively.

Median serum folate was 18% lower and median serum cobalamin was 11% higher in patients with mental disorders compared to controls. Folate deficiency was associated with 54% higher median tHcy levels among patients with mental disorders compared to controls. The prevalence of folate deficiency was 31% and of cobalamin deficiency 6% in patients admitted to a psychiatric acute unit in a Norwegian hospital in 2024.

Folate, but not cobalamin deficiency, was prevalent in Norwegian patients with mental disorders. The higher tHcy levels in folate-deficient patients with mental disorders indicate an impaired folate metabolism, which might be related to genetic factors, such as polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene. Ensuring a serum folate concentration above 15 nmol/L and a serum cobalamin above 250 pmol/L might improve symptoms in patients with mental disorders.

Cognitive function plays a pivotal role in assessing an individual’s quality of life. This research aimed to investigate how azelaic acid (AzA), a natural dicarboxylic acid with antioxidant and anti-inflammatory properties, affects aluminium chloride (AlCl3)-induced behavioural changes and biochemical alterations in the hippocampus of rats.

Thirty-two male Wistar rats divided into four groups received distilled water, AzA 50 mg/kg, AlCl3 100 mg/kg and AzA plus AlCl3, respectively, by oral gavage for 6 weeks. Behavioural changes were evaluated using open-field maze, elevated plus maze, novel object recognition (NOR), passive avoidance task, and Morris water maze (MWM) tests. Also, malondialdehyde (MDA), carbonyl protein, tumour necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), nuclear factor-kappa B (NF-κB), C/EBP homologous protein (CHOP), glycogen synthase kinase-3 beta (GSK-3β), brain-derived neurotrophic factor (BDNF) and acetylcholinesterase (AChE) activity were examined.

AzA significantly affected AlCl3-provoked anxiety-like behaviours and learning and memory impairments. It also reduced the toxic effect of AlCl3 on MDA, carbonyl protein, TNF-α, IL-1β, NF-κB and GSK-3β status; however, its beneficial effects on AlCl3-induced changes of CHOP, BDNF and AChE activity were not significant.

These findings disclosed that AzA could improve behavioural and cognitive function and almost limit the oxidative stress and neuroinflammation caused by AlCl3.